ArticleThe Journal of clinical endocrinology and metabolism2020
Interleukin-6 (IL-6) Activates the NOTCH1 Signaling Pathway Through E-Proteins in Endometriotic Lesions.
Article in The Journal of clinical endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Interleukin-6 as A Useful Predictor of Endometriosis-Associated Infertility: A Systematic Review.International journal of fertility & sterility · 2023Pooled it
- Inflammatory Changes after Medical Suppression of Suspected Endometriosis for Implantation Failure: Preliminary Results.International journal of molecular sciences · 2024Trial
- The iron-ferroptosis axis in bone homeostasis: a potential complementary pathway for osteoporosis in endometriosis.European journal of medical research · 2026Review
- Eutopic Endometrium Immune Changes Involved in Development and Progression of Endometriosis: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.Current molecular medicine · 2026Review
- Serum creatinine as a risk factor for endometriosis: insights from cross-sectional study, mendelian randomization analysis, and diagnostic model study.BMC women's health · 2025Article
- Spatial transcriptomic analysis identifies epithelium-macrophage crosstalk in endometriotic lesions.iScience · 2025Article
- Gallic acid suppresses esophageal squamous cell carcinoma progression and enhances cisplatin chemosensitivity through IL-6/STAT3/Notch pathway.Oncology research · 2025Article
- Macrophages in Calcific Aortic Valve Disease: Paracrine and Juxtacrine Disease Drivers.Biomolecules · 2024Review
- The Known, the Unknown and the Future of the Pathophysiology of Endometriosis.International journal of molecular sciences · 2024Review
- Aberrant activated Notch1 promotes prostate enlargement driven by androgen signaling via disrupting mitochondrial function in mouse.Cellular and molecular life sciences : CMLS · 2024Article
- Potential mechanism of Luoshi Neiyi prescription in endometriosis based on serum pharmacochemistry and network pharmacology.Frontiers in pharmacology · 2024Article
- Digestive system deep infiltrating endometriosis: What do we know.Journal of cellular and molecular medicine · 2023Review
- Detection of Endometriosis Lesions Using Gd-Based Collagen I Targeting Probe in Murine Models of Endometriosis.Molecular imaging and biology · 2023Article
- Spheroids as a model for endometriotic lesions.JCI insight · 2023Article
- Interleukin-6 and pulmonary hypertension: from physiopathology to therapy.Frontiers in immunology · 2023Review
- Review of the Potential Therapeutic Effects and Molecular Mechanisms of Resveratrol on Endometriosis.International journal of women's health · 2023Review
- Peritoneal immune microenvironment of endometriosis: Role and therapeutic perspectives.Frontiers in immunology · 2023Review
- AP-1 Subunit JUNB Promotes Invasive Phenotypes in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Early growth response 1 transcription factor is essential for the pathogenic properties of human endometriotic epithelial cells.Reproduction (Cambridge, England) · 2022Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
contextNOTCH signaling is activated in endometriotic lesions, but the exact mechanisms remains unclear. IL-6, which is increased in the peritoneal fluid of women with endometriosis, induces NOTCH1 through E-proteins including E2A and HEB in cancer.
objectiveTo study the role of E-proteins in inducing NOTCH1 expression under the regulation of IL-6 in endometriosis. SETTING AND
designThe expression of E-proteins and NOTCH1 was first investigated in endometrium of women with endometriosis and the baboon model of endometriosis. Regulation of E-proteins and NOTCH1 expression was examined after IL-6 stimulation and siRNA mediated inhibition of E2A or/and HEB in human endometriotic epithelial cells (12Z) in vitro, and subsequently following IL-6 treatment in the mouse model of endometriosis in vivo.
resultsE2A, HEB, and NOTCH1 were significantly upregulated in glandular epithelium (GE) of ectopic endometrium compared to eutopic endometrium in both women and the baboon model. IL-6 treatment upregulated the expression of NOTCH1 together with E2A and HEB in 12Z cells. Small interfering RNA inhibition of E2A and HEB or HEB alone decreased NOTCH1 expression. Binding efficiency of both E2A and HEB was significantly higher at the binding sites on the human NOTCH1 promoter after IL-6 treatment. Finally, IL-6 treatment resulted in a significantly increased number of endometriotic lesions along with increased expression of E2A, HEB, and NOTCH1 in GE of the lesions compared with the vehicle group in an endometriosis mouse model.
conclusionsIL-6 induced NOTCH1 expression is mediated by E-proteins in the ectopic GE cells, which may promote endometriotic lesion development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.